4.8 Editorial Material

A yeast two-hybrid screening identifies novel Atg8a interactors in Drosophila

期刊

AUTOPHAGY
卷 18, 期 5, 页码 1211-1212

出版社

TAYLOR & FRANCIS INC
DOI: 10.1080/15548627.2022.2045535

关键词

Autophagy; IMD; inflammation; LIR-motif; Sh3px1; Tab2; Tak1

资金

  1. BBSRC [BB/L006324/1, BB/P007856/1, BB/V014838/1]
  2. Leverhulme Trust [RPG-2017-023]
  3. Midlands Integrative Biosciences Training Partnership
  4. BBSRC [BB/V014838/1] Funding Source: UKRI

向作者/读者索取更多资源

Macroautophagy/autophagy-related protein Atg8/LC3 plays a crucial role in autophagosome formation and selective degradation of various substrates. A recent study identified several proteins that interact with Atg8a, the Drosophila homolog of Atg8/LC3. Among these proteins, Tak1 and its co-activator Tab2 were found to interact with Atg8a and be subjected to selective autophagic clearance. Additionally, SH3PX1 was shown to interact with Tab2 and play a role in regulating the immune-deficiency (IMD) pathway. These findings provide insights into the regulatory interactions between Tak1-Tab2-SH3PX1 and Atg8a, contributing to the fine-tuning of the IMD pathway.
Macroautophagy/autophagy-related protein Atg8/LC3 is important for autophagosome biogenesis and required for selective degradation of various substrates. In our recent study, we performed a yeast two-hybrid screening to identify proteins that interact with Atg8a, the Drosophila homolog of Atg8/LC3. The screening identified several Atg8a-interacting proteins. These proteins include: i) proteins which have already been experimentally verified to bind Atg8a, such as Atg1, DOR, ref(2)P and key (Kenny); ii) proteins for which their mammalian homologs interact with Atg8-family members, like Ank2, Atg4, and Nedd4; and iii) several novel Atg8a-interacting proteins, such as trc/STK38 and Tak1. We showed that Tak1, as well as its co-activator, Tab2, both interact with Atg8a and are substrates for selective autophagic clearance. We also determined that SH3PX1 interacts with Tab2 and is necessary for the effective regulation of the immune-deficiency (IMD) pathway. Our findings suggest a mechanism for the regulatory interactions between Tak1-Tab2-SH3PX1 and Atg8a, which contribute to the fine-tuning of the IMD pathway.

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